The intraluminal pressure at the esophagogastric junction (EGJ) is the major barrier to gastroesophageal reflux. Studies until recently suggested that this pressure resulted exclusively from the tonic activity of the smooth muscles of the lower esophageal sphincter (LES). However, recent studies in the animal, as well as humans reveal that skeletal muscles of the crus of the diaphragm provide an external LES-like action at the EGJ. We have proposed that the negative pressure required for ventilatory function of the lung and generated by contraction of the diaphragm causes pressure gradients that will facilitate gastroesophageal reflux. The sphincteric function of the diaphragm is critical in counteracting this increase in the pressure gradient. In support of this theory we found that EGJ pressure in healthy subjects during diaphragmatic contraction is directly proportional and always higher than the gastroesophageal pressure gradient. Our initial work has laid down the grounds in terms of technological capability to accurately record pressures in an axially mobil EGJ. Furthermore, along with this pressure measurement, we can also monitor electrical activity of the diaphragm concurrently. With these capabilities at hand. We are fairly certain that our further studies will help in understanding the mechanism of human LES competence. The aims of our studies not are to define: 1) Characteristics of the diaphragmatic sphincteric action during a relaxed LES, 2) the contribution of the diaphragmatic contraction to pressure at the EGJ during periods of increased intra-abdominal pressure, 3) length tension characteristics of the diaphragm in relation to its sphincteric function, 4) sphincteric function of the diaphragm in patients with reflux esophagitis, and 5) the primary abnormality in patients with achalasia of the esophagus is it the diaphragm or the LES? We propose that these studies will be crucial in defining: 1) The role of hiatal hernia in reflux esophagitis, 2) the association between gastroesophageal reflux and pulmonary symptoms, and 3) the pathogenetic basis of achalasia and maybe the other motility disorders of the esophagus.